A second study, in a different mouse model, has shown that the pharmacological agent rapamycin, which has previously been shown to extend life span in mice, may prevent Alzheimer’s disease in humans. A bacterial product first isolated from the soil on Easter Island, rapamycin is already approved by the U.S. Food & Drug Administration to prevent organ rejection in transplant patients. The first of the two Alzheimer’s studies, was published online on February 23, 2010 in the Journal of Biological Chemistry (A. Caccamo et al.), and showed that rapamycin curbed the effects of Alzheimer’s in one mouse model. The new study, published on April 1 in PLoS ONE, showed similar effects in a completely different mouse model of Alzheimer’s. Both reports came from the University of Texas Health Science Center at San Antonio and collaborating institutions. The second report showed that administration of rapamycin improved learning and memory in a strain of mice engineered to develop Alzheimer's. The improvements in learning and memory were detected in a water maze activity test that is designed to measure learning and spatial memory. The improvements in learning and memory correlated with lower damage in brain tissue. "Rapamycin treatment lowered levels of amyloid-beta-42, a major toxic species of molecules in Alzheimer's disease," said senior author Dr. Veronica Galvan. "These molecules, which stick to each other, are suspected to play a key role in the early memory failure of Alzheimer's."

The first genome of a songbird (the male zebra finch), has been sequenced and has revealed secrets of the relatively rare ability to communicate through “learned vocalizations.” This ability has been documented in just a few other animals, including other songbirds, parrots, hummingbirds, bats, whales, and humans. The ability is lacking in chickens, the only other bird to have had its genome sequenced, and is also absent in female zebra finches. The current research indicates that the ability seems to depend, in part, on the extensive involvement of non-coding RNAs (ncRNAs). A major reason the researchers decided to study the zebra finch genome was the male bird's ability to learn complex songs from its father. At first, a fledgling male finch makes seemingly random sounds, much like the babble of human babies. With practice, the young bird eventually learns to imitate its father's song. Once the bird has mastered the family song, it will sing that song for the rest of its life and pass the song on to the next generation. Though female finches do perceive and remember songs, researchers suggest that their inability to learn songs may be due to differences in sex hormones, as well as chromosomal sex differences affecting the brain. The chicken and zebra finch genomes are similar in many ways. Both have approximately one billion DNA base pairs--roughly one-third the size of a human genome. However, researchers discovered that some genes associated with vocal behavior have undergone accelerated evolution in the finch. For example, they found a disproportionately high number of ion channel genes among the 49 genes in the finch genome that are suppressed, or turned off, in response to song. Human ion channel genes have been shown to play key roles in many aspects of behavior, neurological function, and disease.